6

Respiratory Diseases Among

Dust Exposed Workers
Weihong Chen, Yuewei Liu, Xiji Huang and Yi Rong
Department of Occupational and Environmental Health, School of Public Health,
Tongji Medical College in Huazhong University of Science & Technology
China

1. Introduction
Airborne contaminants occur in the gaseous form (gases and vapours) or as aerosols.
Aerosols may exist in the form of airborne dusts, sprays, mists, smokes and fumes. In the
occupational setting, all these forms may be important because they relate to a wide range of
occupational diseases. Airborne dusts are of particular concern because they are well known
to be associated with classical widespread occupational lung diseases such as the
pneumoconiosis, chronic obstructive pulmonary disease, occupational asthma, etc.
Occupational exposure to dust particles occurs everywhere but is especially prevalent in
low- and middle-income countries. Table 1 shows some examples of the types of dust found
in the work environment.

TYPE OF DUST EXAMPLES

mineral dusts free crystalline silica, coal and cement dusts
metallic dusts lead, cadmium, nickel, and beryllium dusts
other chemical dusts many bulk chemicals and pesticides
organic and vegetable dusts flour, wood, cotton and tea dusts, pollen
biohazards viable particles, moulds and spores
Table 1. Common types of dust in the work envrionment

2. Commonest type of occupation dust particles

2.1 Silica
Silica, also known as silicon dioxide (SiO2), is formed from silicon and oxygen atoms. It has
a melting point of 1,600°C and is a colorless, odorless, and noncombustible solid. Since
oxygen and silicon make up about 75% of the Earth, the compound silica is quite common in
surrounding environment1. Silicates comprise about 25% of known minerals, nearly 40% of
the common minerals, and well over 90% of the earth’s crust[1]. It is found in many rocks,
such as marble, sandstone, flint and slate, and in some metallic ores. Silica can also be in soil,
mortar, plaster, and shingles.
Silica occurs in three forms: crystalline, microcrystalline (or cryptocrystalline) and
amorphous (non-crystalline). "Free" silica is composed of pure silicon dioxide, not combined

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with other elements, whereas silicates (e.g. talc, asbestos, and mica) are SiO2 combined with
an appreciable portion of cations. Crystalline silica exists in seven different forms
(polymorphs), depending upon the temperature of formation. The main 3 polymorphs are
quartz, cristobalite, and tridymite. Quartz is subdivided into alpha and beta forms. In
nature, most quartz is alpha-quartz and alpha-quartz comprises the bulk of crystalline silica.
Quartz is the second most common mineral in the world. Amorphous forms of silica, such
as opal, diatomaceous earth, silica-rich fiberglass, fume silica, mineral wool, and silica glass
(vitreous silica), are generally considered as less harmful[2].
Occupational exposure to crystalline silica can occur in any workplace situation where
airborne dust, containing a proportion of crystalline silica, is generated. Industries where
crystalline silica is present include quarrying, mining, mineral processing (eg drying,
grinding, bagging and handling), slate working, stone crushing and dressing, foundry work,
brick and tile making, some refractory processes, construction work, including work with
stone, concrete, brick and some insulation boards, tunnelling, building restoration and in the
pottery and ceramic industries. Figure 1 shows some of the job processes that generate and
disperse large quantities of respirable silica dusts into the air. Silica dust is an inhalation
hazard. Workers may be at risk of silicosis from exposure to silica dust when high-velocity
impact shatters the sand into smaller, respirable (< 0.5 to 5.0 µm in diameter) dust particles.
From recent reports, more than 23 million workers are exposed to crystalline silica in China

Fig. 1. Job processes that generate and disperse respirable silica dusts into the air

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Respiratory Diseases Among Dust Exposed Workers 133

and more than 10 million in India, as well as over 3 million workers in Europe and at 1.7
million in the United States[3].

2.2 Asbestos
Asbestos is a set of six naturally occurring silicate minerals exploited commercially which
possess high tensile strength, flexibility, resistance to chemical and thermal degradation,
and electrical resistance. Six minerals are defined by the United States Environmental
Protection Agency as "asbestos" including those belonging to the serpentine class chrysotile
and those belonging to the amphibole class amosite, crocidolite, tremolite, anthophyllite and
actinolite[4]. They have different physical and chemical properties but share a fibrous form.
Mineralogists have taken a particle with a length-to-breadth ratio (aspect ratio) of 10:1 or
more to be a fibre. In milled asbestos most of the particles have aspect ratios that range from
5:1 to 20:1 or more and, in the case of chrysotile , mostly greater than 50:1. In medical and
environmental literature a regulated fibre has been defined as a mineral particle with a
length which is at least three times greater than its diameter, of length greater than 5
micrometers and diameters less than 3 micrometres. There are essentially two major
varieties of asbestos viz. serpentine and amphibole. Table 2 shows the species and
varieties[5].

SPECIES VARIETY
Chrysotile Serpentine
Anthophyllite Amphibole
Amosite Amphibole
Actinolite Amphibole
Tremolite Amphibole
Crocidolite Amphibole
Table 2. Asbestos

Asbestos is used for insulation in buildings and as ingredient in a number of products, such
as roofing shingles, water supply lines, fire blankets, plastic fillers, and medical packing, as
well as clutches and brake linings, gaskets and pads for automobiles. Table 3 illustrates
certain kinds of work involve high exposure to asbestos. All forms of asbestos are

work involve high exposure to asbestos

asbestos mining and milling manufacture of asbestos tiles

building demolition manufacture of asbestos fabrics
manufacture of brake linings drywall installation
shipbuilding trades drywall removal
insulation work in construction other asbestos removal
plasterers firefighting
pipe fitters asbestos tile setters
railroad workers aluminum plant workers

Table 3. Certain kinds of work involve high exposure to asbestos

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carcinogenic to humans, and may cause mesothelioma and cancer of the lung, larynx and
ovary. Asbestos exposure is also responsible for other diseases, such as asbestosis (fibrosis of
the lungs), pleural plaques, thickening and effusions.
Currently, about 125 million people in the world are exposed to asbestos at the workplace.
According to the most recent WHO estimates, more than 107 000 people die each year from
asbestos-related lung cancer, mesothelioma and asbestosis resulting from exposure at work.
One in every three deaths from occupational cancer is estimated to be caused by asbestos. In
addition, it is estimated that several thousand deaths annually can be attributed to exposure
to asbestos in the home[6].

2.3 Coal mine dust

Coal is a valuable and plentiful natural global resource. It is found throughout the world.
Coal is classified into four main types or ranks (anthracite, bituminous, subbituminous, and
lignite), depending on the amounts and types of carbon it contains and on the amount of
heat energy it can produce. Coal is mined by two methods: surface mining and
underground mining. The choice of mining method is largely determined by the geology of
the coal deposit. Underground mining currently accounts for a bigger share of world coal
production than opencast. Coal mine dust is a mixture that contains more than 50
substances. The mineral content depends on the particle size of the dust and the coal seam.
The most commonly found minerals in coal mine dust include kaolinite, illite, calcite, pyrite
and quartz (silica). Dust from high rank coals usually contains more silica particles than
dust of lower rank coals. Most workplace exposure to coal dust occurs during mining;
however exposure can also occur during handling of the mined product during cleaning
and blending processes or bulk handling at large coal fired facilities[7].

3. Main respiratory diseases related to occupational dust particles

3.1 Pneumoconiosis
Pneumoconiosis is an occupational lung disease and a restrictive lung disease
caused by the inhalation of dust. A longer, factitious term is
pneumonoultramicroscopicsilicovolcanoconiosis. Depending upon the type of dust, the
disease is given different names:
1. Coal worker’ pneumoconiosis(CWP): caused by inhaling coal dust;
2. Asbestosis: caused by inhaling asbestos;
3. Berylliosis: caused by inhaling beryllium;
4. Kaolin pneumoconiosis: caused by inhaling china clay;
5. Siderosis: caused by inhaling iron oxide;
6. Silicosis: caused by inhaling silica dust;
7. Metallic pneumoconiosis: caused by inhaling barium, cobalt, tin, tungsten dust;
8. Talc pneumoconiosis: caused by inhaling talc dust;
9. Popcorn pneumoconiosis: caused by inhaling fumes produced when manufacturing
microwave popcorn
Some more types of pneumoconiosis include graphite pneumoconiosis, carbon black
pneumoconiosis, talc pneumoconiosis, cement pneumoconiosis, mica pneumoconiosis,
aluminosis, electric welder pneumoconiosis, foundry worker's pneumoconiosis.

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3.2 Silicosis
Silicosis is a form of pneumoconiosis caused by inhalation of crystalline silica dust, and is
marked by inflammation and scarring in forms of nodular lesions in the upper lobes of the
lungs[6] (Figure 2).

Fig. 2. Silicosis showing as nodular mass on a chest x-ray

Silicosis is the commonest occupational lung disease worldwide. It occurs everywhere but is
especially prevalent in low- and middle-income countries. China is the country with the
largest number of silicosis patients, with more than 500,000 cases in records from 1949 to
2010. During 1991 to 2010, more than 6,000 new cases and more than 24,000 deaths occurred
annually. The problem is particularly acute in small-scale mines in China[3]. High risk of
silicosis also reported in other countries. The proportions of gold miners with silicosis
increased from 0.03 to 0.32 for black miners and from 0.18 to 0.22 for white miners in a 33-
year period in South Africa. Among ornamental stone carvers in Brazil, the prevalence of
disease remains over 50 percent. Although U.S. silicosis mortality declined between 1968
and 2002, silicosis deaths and new cases continue to occur, even in young workers[6].
The most common form of silicosis (chronic) will often develop between 15 to 45 years after
first exposure, but certain rare forms of the disease can occur after a single heavy dose or
heavy exposures to a very high concentration of silica in a short period of time. Workers
with Silicosis may have following symptoms: Shortness of breath following physical
exertion, severe and chronic cough, fatigue, loss of appetite, chest pains and fevers.
Silicosis is generally divided into three types as below:
1. Acute Silicosis: Occurs after heavy exposure to high concentrations of silica. The
symptoms can develop within a few weeks or as long as 5 years after the exposure.
2. Chronic Silicosis: Occurs after long term exposure (over 10 years) of low concentrations
of silica dust. This is most common form of the disease, and is often undetected for
many years because a chest X-Ray often will not reveal the disease for as long as 20
years after exposure. This type of the disease severely hinders the ability of the body to
fight infections because of the damage to the lungs, making the person more susceptible
to other lung illnesses, including tuberculosis.
3. Accelerated Silicosis: Occurs after exposure to high concentrations of silica. The disease
develops within 5 to 10 years after exposure.

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136 Respiratory Diseases

The development of silicosis is associated with content of free silica in the dust, type of silica,
concentration of dust, dispersion, years of exposure, prevention and individual factors. The
cumulative dose of silica (respirable dust concentration x crystalline silica content x exposure
duration) is probably the most important factor for the development of silicosis[8].
Pathology
Pathological varieties of silicosis include simple (nodular) silicosis, progressive massive
fibrosis, silicoproteinosis (acute silicosis) and diffuse interstitial fibrosis.
Alveolar macrophages engulf inhaled free silica particles and enter lymphatics and
interstitial tissue. The macrophages cause release of cytokines (tumor necrosis factor- , IL-
1), growth factors (tumor growth factor- ), and oxidants, stimulating parenchymal
inflammation, collagen synthesis, and, ultimately, fibrosis.
When the macrophages die, they release the silica into interstitial tissue around the small
bronchioles, causing formation of the pathognomonic silicotic nodule. These nodules
initially contain macrophages, lymphocytes, mast cells, fibroblasts with disorganized
patches of collagen, and scattered birefringent particles that are best seen by polarized light
microscopy. As they mature, the centers of the nodules become dense balls of fibrotic scar
with a classic onion-skin appearance and are surrounded by an outer layer of inflammatory
cells. In low-intensity or short-term exposures, these nodules remain discrete and do not
compromise lung function (simple chronic silicosis). But with higher-intensity or more
prolonged exposures (complicated chronic silicosis), these nodules coalesce and cause
progressive fibrosis and reduction of lung volumes (total lung capacity, ventilatory
capacity) on pulmonary function tests, or they coalesce, sometimes forming large
conglomerate masses (called progressive massive fibrosis).
Silica quartz crystals in lung tissue can be observed under polarised light microscopy.
Figure 3 illustrates a slide under polarised light microscopy of lung tissue containing
crystalline silica quartz. The white spots represent silica crystals in the specimen of lung
tissue. The silica crystals present in the lung tissue are of different size and represent

Fig. 3. Lung tissue observed under polarized light microscopy containing crystalline silica

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Respiratory Diseases Among Dust Exposed Workers 137

therefore a typical picture of silica crystal distribution in lung tissue of a worker exposed to
crystalline silica.
The primary feature that develops in lungs of silica quartz exposed workers is nodule
formation in the upper zones of the lung[9]. Nodule formation is usually the result of many
years of exposure to relatively low levels of dust that contain silica quartz[10]. Figure 4
represents a photo of silicotic nodule. The classical silicotic nodule is usually located in the
area of the respiratory bronchiole.The nodule is composed of reticulin fibres in the
periphery and collagen fibresin the center. Fibroblastic activity is usually evident around the
periphery of the concentric lesion[11].

Fig. 4. A microscopic photo of a typical silicotic nodule containing collage fibres in a

whorled pattern

The airway and blood vessels are frequently destroyed by being entrapped in the fibrotic
nodule. Silica particles are difficult to identify in tissue section by polarized light
microscopy. Therefore, special techniques involving high resoluton microscopy are
required. It appears that the extent of lesion bears little association with amount of silica
present[11].
Diagnosis
The diagnosis of silicosis generally rests upon history of substantial exposure to silica dusts
and compatible radiological features, together with the exclusion of other competing
diagnoses, like miliary tuberculosis, fungal infections, sarcoidosis, idiopathic pulmonary
fibrosis, other interstitial lung diseases, or carcinomotosis.
History: The individual may report a history of exposure to silica dust. Although initially
there may be no symptoms, symptoms may eventually include difficulty breathing,
shortness of breath, a cough (either dry or productive), and/or chest tightness.

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Physical exam: Auscultation (listening to breath sounds through a stethoscope) may reveal
changes in breath sounds that may indicate obstruction in the upper lobes of the lung.
Wheezing only occurs when other conditions such as bronchitis or asthma are present. In
chronic complicated silicosis or subacute silicosis, right-sided heart failure (cor pulmonale)
may be noted. Rales are often heard.
Tests: Lung tissue changes in progressive silicosis are often detected by chest x-ray before
they cause any symptoms. Pulmonary function tests will be used to evaluate lung function
and confirm the presence of lung disorders. These may include spirometry and lung volume
measurement to detect any restriction of normal lung expansion or obstruction of air flow,
peak flow measurement to detect narrowing of the airways, and diffusing capacity to assess
the efficiency of gas absorption into the blood. Arterial blood gases (ABGs) are performed to
assess the efficiency of gas exchange in the lungs by measuring oxygen and carbon dioxide
(CO2) in arterial blood. CT scanning may also be useful for identifying lung nodules. It’s
generally accepted that the advent of high-resolution computed tomography (HRCT) has
been the major diagnostic technique which is more sensitive than conventional radiography
in detecting nodular lung parenchymal changes, progressive massive fibrosis, bulla,
emphysema, pleural and hilar changes in silicosis. Qualitative and quantitative parameters
on HRCT may also be used as indirect measures of functional impairment in silicosis.
Therefore, HRCT has been widespread used. Sputum (phlegm) may be cultured to identify
any causative organisms and to rule out tuberculosis.
Treatment
Damage to the lungs from silicosis is irreversible; there is no standard treatment other than
reducing symptoms and treating complications. Lung tissue changes due to silicosis are
often detected by a chest x-ray before they cause any symptoms. If dust exposure is stopped
at this point, further progression of the disease can sometimes be prevented.
The disease is otherwise treated symptomatically. Appropriate drug therapy may be given
to control symptoms; these may include drugs to reduce inflammation (anti-inflammatory),
antibiotics to treat or prevent infections, and drugs to widen the airways in the lungs
(bronchodilators). Sleeping in a semi-upright position may help reduce shortness of breath.
Because smoking can aggravate the symptoms of silicosis and increase the risk of lung
cancer, people with the condition who smoke cigarettes are urged to quit. In severe or
advanced cases, a lung transplant may be required[12].
Prevention
Silicosis are preventable. In 1995, the ILO/WHO Global Program for the Elimination of
Silicosis (GPES) was established by a joint ILO/WHO committee. GPES is encouraging and
supporting countries with silica hazard to establish their national action programs to control
silicosis.
It is recommended to assess the potential of silica exposure before a job begins, especially in
the industries where silicosis cases were reported before[13]. Periodic respirable silica
monitoring should be performed in all industries involving silica exposure. Currently
enforced or suggested permissible exposure limits (PEL) for respirable silica are between
0.025 mg/m3 and 0.35 mg/m3 in different countries [14-16]. The current standards have not
been confirmed by epidemiology studies to be fully protective. For example, the

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quantitative risk assessments by NIOSH predicted excess lifetime risks of 19/1000 for lung
cancer mortality, 54/1000 for lung disease other than cancer and 75/1000 for radiographic
silicosis with exposure at the current US Occupational Safety and Health Authority standard
for respirable cristobalite dust (about 0.05 mg/m3) over 45-year working lifetime[17].
For workers in workplaces with high dust levels, administrative measures can also be used
to reduce exposure to silica dust e.g., by cutting short their working hours or job rotation.
Exposure control at the worker level includes training and education on work practices, and
personal protection. Personal protection equipment such as respirators is a good solution for
short duration tasks. Respirators can be used in combination with engineering controls.
However, they should only be considered as the last resort for routine full shift protection.
They cannot be heavily relied upon because they may not be fully effective in workplaces
with high dust concentrations. NIOSH recommends the use of half-facepiece particulate
respirators with N95 or better filters for exposure to crystalline silica at concentrations less
than or equal to 0.5mg/m3 [18].
Regular medical evaluation may detect adverse health effects among exposed workers
before disease reaches advance stages[13].Medical evaluation commonly includes
respiratory questionnaires, physical examination, chest radiography and spirometry. There
is no universal standard as to how frequent such evaluation should be performed, because
the decision may be influenced by past and current respirable silica concentration, dust
particulate characteristics and economic conditions. The WHO recommends routine
evaluation every 2–5 years, ideally ‘life-long’ for workers exposed to silica dust[19].
American College of Occupational and Environmental Medicine (ACOEM) recommended
evaluation at baseline and after 1 year, then 3-yearly for the first 10 years and 2-yearly
thereafter when silicosis is the major concern and respirable silica levels are below 0.05
mg/m3[20]. Biomarkers of early disease could potentially benefit prevention efforts and
clinical diagnosis. While a number of biomarkers have shown some promising results, none
of them have been validated fully for clinical use so far[21]. The occurrence of a new case of
silicosis is a sentinel health event to prompt a thorough evaluation of silica exposure levels
and control measures in workplace[22]. In addition to reporting new cases, occupational
health doctors or hygienists should periodically analyze health records from all workers in
an industry or plant and assess the effects of prevention activities.

3.3 Chronic obstructive pulmonary diseases

In the past few years a new definition has been presented by Global Initiative on
Obstructive Lung Disease (GOLD) and by a Task Force of the American Thoracic Society
(ATS) and the European Respiratory Society (ERS). Both GOLD and ATS/ERS state that
“COPD is a disease state characterized by airflow limitation that is not fully reversible. The
airflow obstruction is usually both progressive and associated with an abnormal
inflammatory response of the lungs to noxious particles and gas.” The ATS/ERS definition
also state that COPD is both preventable and treatable and that COPD is systemic
disease[23].
Epidemiology
According to WHO estimates, 80 million people have moderate to severe chronic
obstructive pulmonary disease (COPD). More than 3 million people died of COPD in 2005,

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which corresponds to 5% of all deaths globally. In 2002 COPD was the fifth leading cause of
death, and expected to become the third leading cause of death globally by 2030, trailing
only ischemic heart disease and cerebrovascular disease[24].
During 2000--2005, COPD was the underlying cause of death for 718,077 persons overall
aged >25 years in the United States. In 2005, approximately one in 20 deaths in the United
States had COPD as the underlying cause[25]. COPD has a prevalence of 4 to 10 percent in
adults in populations in whom lung function has been measured. The National Health
Interview Survey, an annual survey of approximately 40,000 United States households, has
yielded an estimate of 10 million adults in the United States with a physician-based
diagnosis of COPD. Other estimates, such as that from the Third National Health and
Nutrition Examination Survey (NHANES III), that included spirometry along with
questionnaires and a physical examination, done between 1988 and 1994, have yielded even
more impressive prevalence figures. According to NHANES III, COPD affects 23.6 million
adults in the United States, of whom 2.4 million have severe disease. Thus, approximately 10
percent of the United States adult population might be classified as having COPD, and of
this group about 10 percent have advanced disease[23].
According to data published by the Chinese Ministry of Health, COPD ranks as the fourth
leading cause of death in urban areas and third leading in rural areas [16]. The overall
prevalence of COPD in China was 8.2% (95% CI, 7.9–8.6) according to GOLD diagnostic
criteria. The crude prevalence of COPD was the highest in Chongqing and lowest in
Shanghai among urban areas and was highest in Guangdong and lowest in Liaoning and
Shangxi among rural areas. The COPD prevalence was significantly higher in rural areas
compared with urban areas[26]. Both crude and age-adjusted COPD mortality rates have
fluctuated but have displayed a decreasing trend from 1990 which is probably because of
improved management of COPD, upgraded technologies, and awareness of the
disease[24].
Risk factors
There are two types of risk factors for COPD: host factor and exposures (table 4).

ENVIRONMENT EXPOSURES HOST FACTORS

Smoking Genetic mutations
Occupational exposures Airway hyperresponsiveness
Air pollution Reduced lung growth
Childhood respiratory infections
Low socioeconomic status
Table 4. Common risk factors for COPD

Cigarette smoking is the major risk factor for COPD. However, relevant information from
the literature published within the last years, either on general population samples or on
workplaces, indicates that about 15% of all cases of COPD is work-related[27]. A 1989 study
of black goldminers showed that the risk of chronic airflow limitation increases with
duration of underground exposure and is an effect that is independent of the presence of
silicosis. A study of white South African gold miners showed that the forced expiratory

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Respiratory Diseases Among Dust Exposed Workers 141

volume in one second (FEV1), and the FEV1/FVC ratio, adjusted for age, height, and
tobacco smoking, decreased with increasing cumulative respirable dust exposure, in both
smokers and non-smokers. The average cumulative dust exposure attributables loss in lung
function[28].
Pathology
COPD includes two main diseases: bronchitis - in which inflammation of the bronchi (tubes
carrying air to and from the lung) both narrows them and causes chronic bronchial
secretions. Chronic bronchitis is defined by the presence of cough and sputum production
on most days for three or more months of the year for two or more consecutive years[29];
and emphysema - a permanent destructive enlargement of the airspaces within the lung
without any accompanying fibrosis of the lung tissue. Asthma may also be included within
the term COPD if there is some degree of chronic airway obstruction.
In COPD, inflammation causes direct destruction of lung tissues and also impairs defense
mechanisms used to repair damaged tissues. This results in not only destruction of the lung
parenchyma, but also mucus hypersecretion, and airway narrowing and fibrosis.
A wide range of inflammatory cells and mediators are involved in the pathogenesis
of COPD, namely neutrophils, macrophages, and CD8+ T cells in different areas of the
lung.
Overall, COPD pathogenesis can be summarized as resulting from a combination of genetic
susceptibility combined with environmental exposures which lead to inflammatory
processes that disrupt the balance of proteases and antiprotease. These abnormal
inflammatory mechanisms result in tissue destruction, airway inflammation and
remodeling, and ultimately airway limitation. These imbalances and the presence of
inflammation may result in a “positive feedback loop,” in which inflammation induces these
imbalances, and the imbalances promote more inflammation. Once the inflammatory
responses are set in motion, three types of damages to the lung occur: disruption of the
alveolar walls, mucus hypersecretion contributing to airway obstruction, and fibrosis of the
bronchioles.To support the inflammation mechanism further, a study shows there is a
stepwise increase in alveolar inflammation has been found in surgical specimens from
patients without COPD versus patients with mild or severe emphysema. As part of the
peripheral airway system, the bronchioles are the major site of airway obstruction in
COPD[30].
Diagnosis
The diagnosis of COPD, classification of its severity, and progression of the disease can be
monitored with spirometry. A test that measures the forced expiratory volume in one
second (FEV1), which is the greatest volume of air that can be breathed out in the first
second of a large breath. Spirometry also measures the forced vital capacity (FVC), which
is the greatest volume of air that can be breathed out in a whole large breath. Normally, at
least 70% of the FVC comes out in the first second (i.e. the FEV1/FVC ratio is >70%). A
ratio less than normal defines the patient as having COPD. More specifically, the
diagnosis of COPD is made when the FEV1/FVC ratio is <70%. The GOLD criteria also

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require that values are after bronchodilator medication has been given to make the
diagnosis, and the NICE criteria also require FEV1%. According to the ERS criteria, it is
FEV1% predicted that defines when a patient has COPD, that is, when FEV1% predicted is
< 88% for men, or < 89% for women[31]. Once airflow obstruction is established, the
severity of the disease is classified by the reduction of FEV 1 compared with a healthy
reference population. Table 5 shows the widely used GOLD classification of COPD
severity based on the FEV1.

STAGE CHARACTERISTICS
I Mild COPD FEV1 80% predicted
II Moderate COPD FEV1 50% - 79% predicted
III Severe COPD FEV1 30% - 49% predicted
IV Very Severe COPD FEV1 < 30% predicted or < 50% predicted with room air
Pao2 < 60 mmHg (8.0KPa)
Table 5. Classification of COPD severity

On chest x-ray, the classic signs of COPD are overexpanded lung, a flattened diaphragm,
increased retrosternal airspace, and bullae[32]. A high-resolution computed tomography
scan of the chest may show the distribution of emphysema throughout the lungs and can
also be useful to exclude other lung diseases.
Treatment
Directions about the management and prevention of work-related diseases [33-35], can be
applied to COPD as well. Physicians should attempt to understand the patient's
occupational exposure and whether he/she has been adequately trained in the dangers of
these exposures and how to manage them. Removal of the respiratory irritants and
substitution of non-toxic agents are the best approach because they eliminate the work-
related COPD hazard. If substitution is not possible, ongoing maintenance of engineering
controls, such as enclosure of the industrial process and improving work area ventilation,
are useful. Administrative controls (e.g., transfer to another job or change in
work practices), and personal protective equipment (e.g., masks or respirators)
should be mentioned, although less effective in decreasing exposures to respiratory tract
irritants.

3.4 Asthma
Occupational asthma is a lung disorder in which substances found in the workplace cause
the airways of the lungs to swell and narrow, leading to attacks of wheezing, shortness of
breath, chest tightness, and coughing.
Causes and prevalence
Though the actual rate of occurrence of occupational asthma is unknown, it is suspected to
cause 2 - 20% of all asthma cases in industrialized nations. In the USA, OA is considered the
most common occupational lung disease[33]. At present, over 400 workplace substances
have been identified as having asthmagenic or allergenic properties. Their existence and

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magnitude vary from region to region and the type of industry and can be as varied as
wood dust (cedar, ebony, etc.), persulfates (Hairsprays), zinc or even seafood like prawns. In
south-eastern Nigeria, a study was done to determine the magnitude of the problem among
woodworkers exposed to high level of wood dust. Five hundred and ninety one
woodworkers were selected using a stratified random sampling. The prevalence of
occupational rhinitis was 78%, while that of asthma was 6.5%. As period of woodwork
increased the prevalence of rhinitis and asthma increased (rhinitis: chi2 trend = 53.015, df =
1, P = 0.000; asthma, chi2 trend = 19.721, df = 1, P = 0.000). It demonstrates that the
prevalence of rhinitis and asthma in woodworkers was high and significantly increased
with years of working as a woodworker[34].
Occupations at risk
The riskiest occupations for asthma are: adhesive handlers (e.g. acrylate), animal handlers
and veterinarians (animal proteins), bakers and millers (cereal grains), carpet makers
(gums), electronics workers (soldering resin), forest workers, carpenters and cabinetmakers
(wood dust), hairdressers (e.g. persulfate), health care workers (latex and chemicals such as
glutaraldehyde), janitors and cleaning staff (e.g. chloramine-T), pharmaceutical workers
(drugs, enzymes), seafood processors, shellac handlers (e.g. amines), solderers and refiners
(metals), spray painters, insulation installers, plastics and foam industry workers (e.g.
diisocyanates), textile workers (dyes) and users of plastics and epoxy resins (e.g.
anhydrides)[35].
Mechanism
Even if the precise causative mechanism of occupational asthma is unknown, several
mechanisms have been proposed, i.e. immunological, pharmacological and genetic
mechanisms, and airway and neurogenic inflammation. More than one mechanism may
be operative in occupational asthma. Whether various mechanisms are involved in
occupational asthma induced by different agents is also unknown. An agent which causes
asthma may be considered as "inducer" (i.e. causing reversible airway bronchoconstriction
associated with long-lasting airway hyperresponsiveness to nonspecific and/or specific
agents) or as "inciter" (i.e. triggering asthma attacks)[36]. Among the mechanisms
proposed in the pathogenesis of occupational asthma, the immunological one plays a key
role[35].
Diagnosis
Diagnosis of OA is a process and has to be done over a period of time. First, the patient’s
occupational and clinical history is taken and his symptoms are charted (Charting is usually
done at the end of a typical work week and within 24 hours of the occurrence of symptoms
in order to get objective information). Once this has been established, the following
diagnostic methods are used:
1. Blood tests to look for antibodies to the substance;
2. Bronchial provocation test (test measuring reaction to the suspected allergen);
3. Chest x-ray;
4. Complete blood count;

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144 Respiratory Diseases

5. Peak expiratory flow rate;

6. Pulmonary function tests.
Treatment
According to the Canadian Centre for Occupational Health and Safety (CCOHS), better
education of workers, management, unions and medical professionals is the key to the
prevention of OA. This will enable them to identify the risk factors and put in place
preventive measures like masks or exposure limits, etc.
Avoiding exposure to the substance which causes you asthma is the best treatment. The best
option is to change your jobs, or using a respiratory device to protect yourselves is an
alternative option.
Anyone diagnosed with Asthma will have to undergo medical treatment. This is
complementary to either removing or reducing the patient’s exposure to the causal
agents.

3.5 Pulmonary tuberculosis

Pulmonary tuberculosis, or TB, is a communicative disease caused by the bacterium
Mycobacterium tuberculosis and, less frequently, M.bovis. Lesions most often occur in the
lungs.
Species of Mycobacterium are characterized by unusual “acid fast” staining properties,
slow growth, relative resistance to chemical disinfectants, and ability to survive for
decades with cells in the infected animal. The few studies of TB as an occupational hazard
suggest that physicians, nurses, medical laboratory workers, and miners are at increased
risk of TB.
The symptoms of active TB of the lung are coughing, sometimes with sputum or blood,
chest pains, weakness, weight loss, fever and night sweats. Tuberculosis is treatable with a
six-month course of antibiotics.
Epidemiology
Roughly a third of the world's population has been infected with M. tuberculosis, and new
infections occur at a rate of one per second. In 2007, an estimated 13.7 million people had
active TB disease, with 9.3 million new cases and 1.8 million deaths; the annual incidence
rate varied from 363 per 100,000 in Africa to 32 per 100,000 in the Americas[37]. In 2007, the
country with the highest estimated incidence rate of TB was Swaziland, with 1200 cases per
100,000 people. India had the largest total incidence, with an estimated 2.0 million new
cases[37]. According to the statistic data released by the Chinese Ministry of Health in July
2011, the recorded cases of pulmonary tuberculosis is 112647 which is the second in the
recorded cases of notifiable disease, and 170 deaths.
However, few studies of TB incidence among various occupational have been reported.
Therefore, only general and somewhat unsatisfactory comments can be made about TB as an
occupational hazard.

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Respiratory Diseases Among Dust Exposed Workers 145

Miners and others who work in poorly ventilated areas are more likely to be infected by a
fellow worker who has TB than a person who works in a well-ventilated areas[38].
Silicotuberculosis
Both silica dust exposure and silicosis are risk factors for TB. Tuberculosis in a person with
established silicosis is termed silicotuberculosis. The risk of developing TB increases with
duration of exposure to silica dust even in the absence of silicosis. The presence of silicosis
increases the risk of pulmonary TB approximately four fold, with the risk rising as
radiological become more severe. This increased risk of TB associated with silicosis is
lifelong, continuing after silica exposure ceases.
The presence of silicosis in the lungs can be modify the natural history of TB and may alter
its radiological appearance. The interaction of TB and silicosis is very damaging to the lung,
unless the TB is diagnosed and treated early.
Pathology
Infection with Mycobacterium tuberculosis results most commonly from infected aerosol
exposure through the lungs or mucous membranes. In immunocompetent individuals, this
usually produces a latent/dormant infection, only about 5% of these individuals later show
evidence of clinical disease.
TB infection begins when the mycobacteria reach the pulmonary alveoli, where they invade
and replicate within the endosomes of alveolar macrophages[39]. The primary site of
infection in the lungs is generally located in either the upper part of the lower lobe, or the
lower part of the upper lobe[39]. Bacteria are picked up by dendritic cells, which do not
allow replication, although these cells can transport the bacilli to local (mediastinal) lymph
nodes. Further spread is through the bloodstream to other tissues and organs where
secondary TB lesions can develop in other parts of the lung (particularly the apex of the
upper lobes), peripheral lymph nodes, kidneys, brain, and bone[40].
Workers exposed to silica are more likely to have TB because silica interferes with the
function of the pulmonary macrophages[38].
Diagnosis and Treatment
The diagnosis of tuberculosis is confirmed by the growth of Mycobacterium tuberculosis from
culture of sputum, CSF, urine, lymph nodes, or other infected tissue. If necessary, the
patient should have a positive tuberculin shin test.
The goal of treatment is to cure the infection with drugs that fight the TB bacteria. Treatment
of active pulmonary TB will always involve a combination of many drugs (usually four
drugs). All of the drugs are continued until lab tests show which medicines work best. The
most commonly used drugs include: Isoniazid, Rifampin, Pyrazinamide and Ethambutol.
Prevention
Transmission of TB can be prevented by the rapid identification and treatment of persons
with disease and by the identification and treatment of those persons infected but not yet
diseased.

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146 Respiratory Diseases

As indicated above, chronic inhalation of dust particles has been linked for decades with
lung diseases such as silicosis and silicotuberculosis. Also studies have suggested that dust
particles may increase risk of lung cancer as well as some other diseases.

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[3] NIOSH Hazard Review. Health Effects of Occupational Exposure to Respirable Crystalline
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[4] Berman, D.W.C., Kenny S, Final draft:technical support document for a protocol to assess
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[5] R. Guild, R.I.E., Airbone pollutants: asbestos. Occupational health practice in the South
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[7] Coal Dust at the Work Site. CH063 — Chemical Hazards. Government of Alberta, April
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[10] MM., F., Silica, silicosis, and lung cancer: a risk assessment. Am.J Ind.Med, 2000. 38(1):8-18.
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diseases, 1986: p. 230.
[12] preventing silicosis. Centers for Disease Control and Prevention. U.S. Department of
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[15] American Conference of Governmental Industrial Hygienists. Cincinnati: ACGIH, 2009.
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Silica. Washington D.C.: DHHS Publication, 2008. No. 2008-140.

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Respiratory Diseases Among Dust Exposed Workers 147

[19] Wagner G, W.S., Screening and surveillance of workers exposed to mineral dust. Geneva:
World Health Organization, 1996.
[20] Raymond, L.W. and S. Wintermeyer, Medical surveillance of workers exposed to crystalline
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[22] Aldrich, T.E. and P.E. Leaverton, Sentinel event strategies in environmental health. Annu
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African mining industry, 2001: p. 131.
[30] D., P., The pathogenesis and pathology of COPD: identifying risk factors and improving
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[31] Alleman, J.E., Asbestos Revisited. Scientific American November 2010. 54-57.
[32] M., T., Evaluation of the acutely dyspneic elderly patient. Clin. Geriatr. Med, May 2007. 307–
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[33] Bonauto, D., Diagnosing Work-Related Asthma. American College of Occupational and
Environmental Medicien, 2006.
[34] Aguwa, E.N., T.A. Okeke, and M.C. Asuzu, The prevalence of occupational asthma and
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[35] C.E. Mapp, M.S., Mechanisms and pathology of occupational asthma. Eur Respir J, July 1993.
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[36] Dolovich, J. and F. Hargreave, The asthma syndrome: inciters, inducers, and host
characteristics. Thorax, 1981. 36(9): p. 614-44.
[37] Global tuberculosis control: epidemiology, strategy, financing. World Health Organization
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[38] James A . Merchant, M.D., Dr. P.H., Tuberculosis as an occupational disease. Occupational
respiratory diseases, 1986: p. 709.

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148 Respiratory Diseases

[39] Kumar V, A.A., Fausto N, Robbins Basic Pathology Saunders Elsevier: p. 516–522.
[40] Herrmann J, L.P., Dendritic cells and Mycobacterium tuberculosis: which is the Trojan horse?.
. Pathol Biol 53 (1): p. 35–40.

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 Respiratory Diseases
Edited by Dr. Mostafa Ghanei

ISBN 978-953-307-964-6
Hard cover, 242 pages
Publisher InTech
Published online 01, February, 2012
Published in print edition February, 2012

Medicine is an ever-changing science. In this regard, Respiratory medicine is not an exception and has been
evolving during recent years. As new research broadens our knowledge, advanced methods for diagnoses are
better understood, providing genetic and underlying pathophysiology of diseases and new clinical experiences.
Consequently, publications of new resources along with revisions of previous ones are required. The book
Respiratory Diseases brings practical aspects of pulmonary diseases. It contains the result of years of
experience through expert clinicians in this field from different scientific centers. The respiratory diseases are
discussed according to epidemiology, pathology, diagnosis, treatment, and prognosis. It includes updated
resources of the pathogenesis and some molecular aspects of the aforementioned diseases and is
recommended reading for all clinicians and medical students, especially pulmonologists, to access highlighted
respiratory diseases in this book.

How to reference
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Weihong Chen, Yuewei Liu, Xiji Huang and Yi Rong (2012). Respiratory Diseases Among Dust Exposed
Workers, Respiratory Diseases, Dr. Mostafa Ghanei (Ed.), ISBN: 978-953-307-964-6, InTech, Available from:
http://www.intechopen.com/books/respiratory-diseases/respiratory-diseases-among-dust-exposed-workers

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